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blood transfusion check

Image: “Hospital Corpsman Megan Beach, checks the flow of blood through a cell saver, during training for an antilogous blood transfusion aboard Military Sealift Command (MSC) hospital ship USNS Mercy (T-AH 19).” by U.S. Navy photo by Journalist Seaman Apprentice Mike Leporati. License: Public Domain

Patient-Induced Emergencies

Massive hemorrhage is a major cause of preventable mortality. The leading causes of massive hemorrhage are as follows:

  • Trauma or assault: the coagulopathy that occurs in the setting of trauma is unique in its pathogenesis, aided by tissue injury factors. It can occur in the absence of significant fluid administration, clotting factor depletion or hypothermia.
  • Vascular disease such as ruptured aneurysm: fortunately seldom, sudden loss of blood volume in such situations makes them potentially lethal.
  • Genetic bleeding disease like hemophilia
  • Postpartum hemorrhage: evidence suggests the presence of an acquired fibrinogen deficiency state, complicated by dilutional coagulopathy and exaggerated fibrinolysis in these patients.
  • Drug-induced hemorrhage: this is a known complication of blood thinners and anti-platelet drugs and an adverse effect of some drugs, such as gastrointestinal hemorrhage secondary to NSAIDs.
  • Surgical error: unexpected damage to a vessel is a potential cause of intra-operative blood loss.

Hemorrhage is classified as anticipated or unanticipated:

Situations in which hemorrhage
Can be anticipated May me completely unexpected
  • Cardiac surgery
  • Vascular surgery
  • Spine surgery
A bleeding disorder is not recognized prior to surgery

Major surgical interventions like cardiac, spine and vascular surgeries have an inherent risk of blood loss and give time for anticipatory preparation. However, unexpected circumstances like undetected bleeding disorder may occur.

Massive Transfusion Protocol

symptoms of acidosis

Image: “General symptoms of acidosis.” by Häggström, Mikael. “Medical gallery of Mikael Häggström 2014”. Wikiversity Journal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 20018762. License: Public Domain

Designed to break through the vicious lethal triad of coagulopathy, acidosis and hypothermia, Massive Transfusion Protocol (MBT) calls for aggressive and rapid judicious use of blood and blood derivatives for the management of a massive hemorrhage to ensure an improved outcome.

MBTs have developed as a collaborative effort between anesthesiologists, surgeons, transfusion medicine physicians, emergency physicians, and intensivists.

The development of evidence-based MBT,  is important to ensure standard approaches to timely detection of hemorrhage and to ensure that appropriate management is initiated.

Currently, these are included in MBT:

Replacement of one entire blood volume within 24 hours

Transfusion of >10 units of packed red blood cells (PRBCs) in 24 hours

Transfusion of >4 units of PRBCs in 1 hour, when the on-going need is foreseeable

Replacement of 50% of total blood volume (TBV) within 3 hours.

Once MTP is initiated, a batch of 5 red blood cells, 5 platelets and 2 fresh frozen plasma (FFP) are to be dispatched. Further batches of blood and blood products are dispatched until needed.

The pre-requisites for successful MTP are:

Intravenous access: Large bore peripheral intravenous access is at the heart of any successful resuscitation. Special insertion sheaths in neck veins may be used, subject to the accessibility and expertise of the team.

Temperature control: warming devices, surface warmers, and core temperature monitors. With transfusion of 2 or more blood products, it is of crucial importance to warm blood products gradually, “thawing“ them to body temperature, prior to transfusion, to prevent complications secondary to a massive infusion of stored blood products like “Disseminated Intravascular Coagulation (DIC)

Central venous pressure monitoring.

Onsite testing such as arterial blood gas and thromboelastography is highly desirable.

Increasing use of blood thinners, especially in the elderly population, has led to rising in transient coagulopathy-like states during surgery.

Ideally, warfarin and similar vitamin K antagonists should be stopped 5-7 days prior to any surgical intervention, bridging the gap with heparin. PT/INR should be monitored and heparin is to be stopped a day prior as per the surgical specifications.

In case of an emergency, prothrombin plasma concentrates (PCC) are used to reverse warfarin effects.

Heparin antidote is protamine sulfate. Newer fractionated low molecular weight heparin formulations are difficult to reverse.

Antiplatelet agents like aspirin and clopidogrel, are withheld (with the consent of the treating physician) and appropriately replaced with heparin if necessary.

Low dose aspirin leads to minimal, if any, increase in bleeding tendency.

Alternative strategies:

tranexamic acid structural formula

Image: “Structural Formula of Tranexamic Acid.” by Jü – Own Work. License: Public Domain

Activated factor VII: benefit in uncontrolled bleeding unresponsive to standard hemostatic therapy is equivocal.

Antifibrinolytic agents: early administration of drugs such as tranexamic acid has a mortality benefit in trauma and obstetric hemorrhages.

Cell salvage: of use in patients with rare blood groups and unexpected massive hemorrhages and feasible in aseptic environments such as operating suites, cell savage carries a potential risk of malignant cells dissemination and contamination.

Complications of MTP:

Overzealous rapid correction without due central venous pressure monitoring can potentially lead to circulatory overload, interstitial edema, and pulmonary edema. There is usually a drop in oxygen saturation that heralds the development of pulmonary edema, associated with high morbidity and mortality. Aggressive diuretic use with curtailed intravenous fluid administration is critical.

Other complications are outlined below:

Immediate complication Intermediate complication Long term complication
Acidosis TRALI (transfusion-related acute lung injury) Renal failure
Hypomagnesemia Cardiac toxicity is secondary to hypocalcemia, hyperkalemia and other factors. Respiratory failure
Hyperkalemia Disseminated intravascular coagulation (consumptive coagulopathy) SIRS (systemic inflammatory response syndrome)
Citrate toxicity Interstitial edema Thrombotic complications
Hypothermia Transfusion-related circulatory overload Sepsis
Hypocalcemia Pulmonary edema
Dilutional coagulopathy

Limitations of Massive Transfusion Protocols

Inappropriate initiation of MTP leads to a waste of energy and resources.

Protocols vary from institution to institution.

Raised Intracranial Pressure

The skull is a rigid, non-compressible limiting element for the intracranial contents. The intracranial space of about 1700 ml is distributed as follows: Brain parenchyma 1400 ml, blood 150 ml and CSF about 150 ml. These intracranial elements are all in a balanced yet flexible dynamic state of equilibrium. If anyone of these elements changes, the others compensate for the change. This principle has been formally addressed as the Monro-Kellie doctrine. However, decompensation of this balance, leading to raised intracranial pressure, as in presence of SOL (space-occupying lesion as tumors), hydrocephalus (increase in CSF component) and extra-axial blood aggregation as in trauma and brain hemorrhage has abysmal effects on cerebral perfusion leading to ischemia and parenchymal damage.

Cerebral blood flow autoregulation, in normal circumstances, ensures adequate cerebral perfusion over a wide range of intracranial pressure. Autoregulation is often impaired in the presence of intracranial space-occupying lesions, trauma, and infection.

Clinical reflection of raised intracranial pressure is the Cushing’s triad: hypertension, bradycardia, and irregular respiration. Cushing’s triad is the brain’s last-ditch effort to maintain cerebral perfusion in the face of increasing cerebral edema.

Increased intracranial pressure in these circumstances leads to the invariably fatal complication of herniation, the herniation of posterior fossa contents, brain stem and cerebellar tonsils through the foramen magnum leading to compression of the critical medullary cardiovascular regulatory centers.

Raised intracranial pressure calls for rapid emergent co-ordinated management.

Intubation: The first traditional step in resuscitation is to control the airway and avoid hypoxia. However, subtle stimulation of the vocal cords can lead to a raised intracranial pressure, tachycardia and hypertension.

Anesthesia drugs have variable effects on intracranial pressure. In the face of impaired autoregulation, some analgesics and sedatives can also lead to major changes in intracranial pressure, cerebral blood flow and cerebral metabolism. Inappropriate naïve use of these drugs can lead to clinical deterioration.

Decongestant drugs, which ameliorate intracranial pressure, are prone to reducing cerebral blood flow below critical levels with resultant cerebral hypoperfusion and elevated risk of ischemic hypoxic encephalopathy and brain damage. Therefore, these agents must be used very cautiously to try to achieve a balance between intracranial pressure and cerebral perfusion. Various drugs and their effects are summarized below :

Drug Effect
Hypnotic agents: propofol Reduction of cerebral blood flow, decrease in cerebral metabolism, decrease ICP, decrease in cerebral perfusion pressure
Benzodiazepines: lorazepam, diazepam Reduction of cerebral blood flow, decrease in cerebral metabolism, decrease ICP, decrease in cerebral perfusion pressure
Opioids: fentanyl, sufentanil Reduction of cerebral blood flow, decrease in cerebral metabolism, no change in ICP; increase in blood volume can lead to a secondary increase in ICP.
Alpha-2 adrenergic agonists: clonidine Reduction of cerebral blood flow, no change in cerebral metabolism, no change in ICP; occasional transient decrease in ICP with low dose
Ketamine Region-specific variable response of blood flow, the variable response of cerebral metabolism, increases ICP
Diuretics: furosemide, mannitol Reduce ICP, reduce cerebral blood flow, decrease cerebral perfusion pressure

Cardiac Disease

Cardiovascular diseases are the leading cause of mortality. Cardiac disease like ischemic heart disease, arrhythmias and severe vascular diseases like aortic stenosis, can lead to heart failure and eventually cardiac arrest.

Cardiac arrest can also be the culmination of pulmonary embolism, tension pneumothorax, cardiac tamponade or hypovolemic shock.

The Advance Cardiac Life Support (ACLS) guidelines published in 2015 (valid through to 2020), provide a protocol, to initiate resuscitation. In the OR, the surgeon is responsible for initiating CPR (cardio-pulmonary resuscitation) and the anesthesiologist for managing the drug administration and patient monitoring. The latter is inclusive of ECG interpretation, monitoring oxygen saturation, end-tidal carbon dioxide and checking for signs of airway obstruction and respiratory issues.

Ventricular arrhythmias like pulseless ventricular tachycardia and ventricular fibrillation call for the use of defibrillation.

Atrial arrhythmias are common, usually benign and often managed without taking recourse to the management of cardiac arrest.

Some salient features of ACLS pertinent to anesthesiology are as follows:

Low-end tidal CO2 (ETCO2 < 10mm Hg) after 20 minutes of CPR in conjunction with other parameters helps determine when to terminate resuscitation.

Extracorporeal CPR can prolong viability if implemented soon after arrest.

Avoidance of immediate correction of hypotension is recommended during post-cardiac arrest care.

In the absence of hypoxia or respiratory distress, oxygen administration is rather to be withheld in patients with acute coronary syndrome.

Patients in cardiac arrest with no definite pulse are to be given focused high-quality CPR with naloxone.

Doctor Induced Emergencies

Wrong Drug and Wrong Dose Errors

A medication error is defined as “treatment process fallacy that potentially culminates in harm to the patient”. Drug errors are the commonest misadventures suffered by patients in hospitals. There are different tiers of medication errors:

Prescribing faults: over and under-prescribing

Prescription errors: the fault in writing prescriptions, illegibility, wrong drugs

Manufacturing errors: adulterants

Dispensing errors: wrong drug, wrong formulation

Administering errors: wrong dosage, wrong access, and wrong frequency.

Medication errors occur in anesthesia.  Timely recognition helps correct untoward hemodynamic changes that may have occurred and evaded an adverse event.

Measures to prevent medication errors for anesthesiologists include:

All syringes are labeled with the drug name and concentration

No syringe to be used in more than one patient

Careful monitoring of the use of controlled drugs

Computerized physician order entry system: These computer-generated programs have built-in warnings about possible drug interactions, duplication of orders, incorrect dose and patient allergies.

Constant vigilance is needed to minimize errors, including careful prescription, administration, and expert observation after administration to avoid potential complications.

Surgical Errors

Surgical care is an indispensable part of medical care.

Surgical errors include:

Wrong side surgery (operating on the incorrect side of the patient)

Inadvertent opening of cavities such as inadvertent bowel perforation, leading to contamination and peritonitis

Vessel damage leading to hemorrhage.

While addressing the safety of surgical care, WHO, in 2007, took up the challenge of reinforcing “Safe Surgery Saves Lives”. At the heart of this WHO, the initiative is the WHO Safe Surgery Checklist. Three phases of the surgical procedure are addressed in this checklist:

Before induction of anesthesia: “Sign in”

Before incision of the skin: “Time out”

Before the patient leaves the operating room: “Sign out”.

In each phase, a checklist co-ordinator checks various points to ensure complete surgical safety. A few salient points are as follows:

Confirm patient identity

Confirm the side of surgery whenever applicable and mark the side

Complete instrument count, mop count

All anticipated complications are to be listed beforehand to avoid unpleasant surprises intra-operatively.

The aim is to follow a few critical steps and thus to avoid infrequent, yet persistent, mishaps that may endanger the well-being of surgical patients.


Patient-induced emergencies include massive hemorrhage, increased intracranial pressure, and cardiac disease.

Doctor-induced emergencies comprise of wrong drug and wrong dose administration and surgical errors.

A massive hemorrhage demands objective massive transfusion protocol based rapid judicious management in order to successfully revive the patient avoiding inherent risks of the protocol.

Anesthetic drugs have to be used wisely in situations with increased intracranial pressure to ensure adequate cerebral perfusion with decreased intracranial tension.

Cardiac disease constitutes common emergencies and has to be managed as per the ACLS guidelines.

Doctor induced errors are common, but mostly trivial and inconsequential if managed at the right time. Expert emergent, conscious, careful management to avoid patient harm should be the goal.


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